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Research Paper|Volume 10, Issue 11|pp 3486—3506

Phosphatidylcholine could protect the defect of zearalenone exposure on follicular development and oocyte maturation

Fang-Nong Lai1, Xue-Lian Liu1, Na Li1, Rui-Qian Zhang1, Yong Zhao1, Yan-Zhong Feng2, Charles Martin Nyachoti3, Wei Shen1, Lan Li1
  • 1College of Life Sciences, Institute of Reproductive Sciences, Qingdao Agricultural University, Qingdao 266109, China
  • 2Institute of Animal Sciences, Heilongjiang Academy of Agricultural Sciences, Harbin, Heilongjiang 150086, China
  • 3Department of Animal Science, University of Manitoba, Winnipeg MB R3T 2N2, Canada

* * Equal contribution

Received: July 26, 2018Accepted: November 15, 2018Published: November 25, 2018

Copyright: © 2018 Lai et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Zearalenone (ZEA) is a well-known exogenous endocrine disruptor and can lead to severe negative effects on the human and animal reproductive process. Using a follicle culture model, we have previously shown that ZEA exposure significantly affected the follicular development and antrum formation but the underlying mechanisms are not well known. Therefore, in this study, we explored the metabolomic changes of granulosa cell (GC) culture media with or without ZEA exposure. The results showed that ZEA significantly increased phosphatidylcholine or phosphatidyl ethanolamine adducts in culture medium. A comprehensive analysis with the metabolome data from follicular fluid of small and large antral follicles showed that lyso phosphatidylcholine (LPC) was accumulated during follicle growth, but was depleted by ZEA exposure. Exogenous supplement with LPC to the follicle growth media or oocyte maturation media can partly protect the defect of ZEA exposure on follicular antrum formation and oocyte maturation. Taken together, our results demonstrate that ZEA exposure hinders the follicular growth and exogenous LPC can practically protect the defect of ZEA on follicular development and oocyte maturation.